Negative regulation of inducible nitric-oxide synthase expression mediated through transforming growth factor-beta-dependent modulation of transcription factor TCF11

Inducible nitric-oxide synthase (iNOS) plays a central role in the regulation of vascular function and response to injury. A central mediator controlling iNOS expression is transforming growth factor-beta (TGF-beta), which represses its expression through a mechanism that is poorly understood. We ha...

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Bibliographic Details
Published in:	The Journal of biological chemistry Vol. 282; no. 51; p. 36837
Main Authors:	Berg, David T, Gupta, Akanksha, Richardson, Mark A, O'Brien, Lee A, Calnek, David, Grinnell, Brian W
Format:	Journal Article
Language:	English
Published:	United States 21.12.2007
Subjects:	Animals Carcinogens - pharmacology Cells, Cultured Dimerization Disease Models, Animal Endotoxemia - enzymology Endotoxemia - genetics Enzyme Inhibitors - pharmacology Gene Expression Regulation, Enzymologic - drug effects Gene Expression Regulation, Enzymologic - genetics Hepatocyte Nuclear Factor 1-beta - antagonists & inhibitors Hepatocyte Nuclear Factor 1-beta - genetics Hepatocyte Nuclear Factor 1-beta - metabolism Humans Inflammation - enzymology Inflammation - genetics MafG Transcription Factor - genetics MafG Transcription Factor - metabolism Male Mutation Naphthalenes - pharmacology Nitric Oxide Synthase Type II - biosynthesis Nitric Oxide Synthase Type II - genetics Protein Kinase C - antagonists & inhibitors Rats Rats, Sprague-Dawley Repressor Proteins - genetics Repressor Proteins - metabolism Response Elements - genetics RNA, Small Interfering - genetics RNA, Small Interfering - pharmacology Signal Transduction - drug effects Signal Transduction - genetics Smad6 Protein - genetics Smad6 Protein - metabolism Smad7 Protein - genetics Smad7 Protein - metabolism Staurosporine - pharmacology Tetradecanoylphorbol Acetate - pharmacology Transforming Growth Factor beta1 - metabolism Transforming Growth Factor beta1 - pharmacology
ISSN:	0021-9258
Online Access:	Get more information
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